JACC: CLINICAL ELECTROPHYSIOLOGY VOL. 8, NO.

1, 2022

ª 2022 BY THE AMERICAN COLLEGE OF CARDIOLOGY FOUNDATION

PUBLISHED BY ELSEVIER

STATE-OF-THE-ART REVIEW

Arrhythmias in Pregnancy
Kamala P. Tamirisa, MD,a Uri Elkayam, MD,b,c Joan E. Briller, MD,d Pamela K. Mason, MD,e
Jayasree Pillarisetti, MD, MSC,f Faisal M. Merchant, MD,g Hena Patel, MD,h Dhanunjaya R. Lakkireddy, MD,i
Andrea M. Russo, MD,j Annabelle Santos Volgman, MD,k Marmar Vaseghi, MD, PHDl

ABSTRACT

Increasing maternal mortality and incidence of arrhythmias in pregnancy have been noted over the past 2 decades in the
United States. Pregnancy is associated with a greater risk of arrhythmias, and patients with a history of arrhythmias are at
significant risk of arrhythmia recurrence during pregnancy. The incidence of atrial fibrillation in pregnancy is rising. This
review discusses the management of tachyarrhythmias and bradyarrhythmias in pregnancy, including management of
cardiac arrest. Management of fetal arrhythmias are also reviewed. For patients without structural heart disease, b-
blocker therapy, especially propranolol and metoprolol, and antiarrhythmic drugs, such as flecainide and sotalol, can be
safely used to treat tachyarrhythmias. As a last resort, catheter ablation with minimal fluoroscopy can be performed.
Device implantation can be safely performed with minimal fluoroscopy and under echocardiographic or ultrasound
guidance in patients with clear indications for devices during pregnancy. Because of rising maternal mortality in the
United States, which is partly driven by increasing maternal age and comorbidities, a multidisciplinary and/or integrative
approach to arrhythmia management from the prepartum to the postpartum period is needed.
(J Am Coll Cardiol EP 2022;8:120–135) © 2022 by the American College of Cardiology Foundation.

A n increasing trend in maternal mortality has

been reported in the United States. As of
2019, an estimated 20.1 maternal deaths per
100,000 live births were reported in the United
States, an increase of 17.4 deaths per 100,000 live
births since 2018, with a growing trend noted since
1999 (1,2). The exact contribution of arrhythmias to
this rising mortality is unclear, because arrhythmias
are not analyzed separately from other cardiovascular
etiologies in the Pregnancy Mortality Surveillance
System (3). However, the incidence of arrhythmias
during pregnancy has also been reported to be
increasing during this same period, primarily caused
by increased incidences of atrial fibrillation (AF) and
ventricular tachycardia (VT). Notably, hospitalization
during pregnancy for arrhythmias is associated with
an increased risk of both maternal and fetal complica-
tions, including maternal mortality (4-6). In a 10-year
retrospective analysis of maternal cardiovascular
deaths, arrhythmias were the immediate or underly-
ing cause in 10.7% (7). The frequency of arrhythmias
is greater in women 41-50 years of age, African

From the aTexas Cardiac Arrhythmia Institute, Austin and Dallas, Texas, USA; bDivision of Cardiology, Department of Medicine,
Keck School of Medicine, University of Southern California, California, USA; cDepartment of Obstetrics and Gynecology, Keck
School of Medicine, University of Southern California, California, USA; dDivision of Cardiology, Department of Medicine, Uni-
versity of Illinois at Chicago, Chicago, Illinois, USA; eDivision of Cardiology, Department of Medicine, University of Virginia,
Charlottesville, Virginia, USA; fDivision of Cardiology, Department of Medicine, University of Texas Health, San Antonio, Texas,
USA; gDivision of Cardiology, Department of Medicine, Emory University School of Medicine, Atlanta, Georgia, USA; hDivision of
Cardiology, Department of Medicine, University of Chicago, Chicago, Illinois, USA; iKansas City Heart Rhythm Institute, Kansas
City, Kansas, USA; jDivision of Cardiology, Cooper University Hospital, Camden, New Jersey, USA; kDivision of Cardiology,
Department of Medicine, Rush University Medical Center, Chicago, Illinois, USA; and the lUCLA Cardiac Arrhythmia Center, Di-
vision of Cardiology, Department of Medicine, University of California, Los Angeles, California, USA.
Anne Curtis, MD, served as Associate Guest Editor for this paper. William Stevenson, MD, served as Guest Editor-in-Chief for this
paper.
The authors attest they are in compliance with human studies committees and animal welfare regulations of the authors’
institutions and Food and Drug Administration guidelines, including patient consent where appropriate. For more information,
visit the Author Center.

Manuscript received June 23, 2021; revised manuscript received October 6, 2021, accepted October 13, 2021.

ISSN 2405-500X/$36.00 https://doi.org/10.1016/j.jacep.2021.10.004

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JACC: CLINICAL ELECTROPHYSIOLOGY VOL. 8, NO. 1, 2022 Tamirisa et al 121
JANUARY 2022:120–135 Arrhythmias in Pregnancy

forms of arrhythmias, such as premature ABBREVIATIONS

HIGHLIGHTS AND ACRONYMS
atrial and ventricular contractions, demon-

The United States reported the highest strate a higher burden during pregnancy
AAD = antiarrhythmic drug
maternal mortality ratio in 2018. compared with prepregnancy. A history of
AF = atrial fibrillation
Arrhythmia incidence during pregnancy arrhythmias is an important risk factor for
CPR = cardiopulmonary
has been increasing. recurrent arrhythmias during pregnancy (15).
resuscitation
New-onset VT can be observed in structurally

Pregnancy is associated with increased DCCV = direct-current
normal hearts (16,17). Proarrhythmic mecha- cardioversion
arrhythmia burden, and patients with a
nisms of pregnancy are presumably related to
ICD = implantable
history of arrhythmias are at significant
cardiovascular, autonomic, and hormonal cardioverter-defibrillator
recurrence risk.
changes. Increased plasma catecholamine SCA = sudden cardiac arrest

Management of tachyarrhythmias de- concentrations, chronotropic effects of SVT = supraventricular
pends on the presence of underlying relaxin, mechanical effects of atrial stretch, tachycardia

structural heart disease and includes increased ventricular end-diastolic volume VT = ventricular tachycardia

adenosine, b -blockers, and specific anti- caused by intravascular volume expansion,

arrhythmic drugs with safety data during and hormonal and emotional changes all contribute
pregnancy. As a last resort, catheter to proarrhythmia (18,19).
ablation with minimal fluoroscopy can be Heart rate progressively increases during preg-
used. nancy, resulting in a 10%-25% increase from pre-
pregnancy values (20). Cardiac output rises early in

Because of rising maternal mortality in
the first trimester and peaks in the second trimester,
the United States, which is partly driven
increasing by 45% (21). Estrogen and relaxin stimulate
by increasing maternal age and comor-
nitric oxide production, which increases peripheral
bidities, a multidisciplinary and/or inte-
arterial compliance and decreases vascular resistance
grative approach from prepregnancy to
(22,23). Normal pregnancy is associated with
postpartum is needed.
decreased parasympathetic and increased sympa-
thetic activity at rest. Increased sympathetic activity
American women, and those in the lowest income
may contribute to abnormal automaticity, reentry, or
quartile compared with Caucasian women, those
triggered activity (24-26).
younger than 30 years of age, and those with higher
socioeconomic status (6). In addition to advanced
ELECTROCARDIOGRAPHIC CHANGES
maternal age and socioeconomic status, underlying
OF PREGNANCY
cardiovascular disease and congenital heart disease,
and cardiovascular comorbidities (hypertension, dia-
Certain electrocardiographic changes have been
betes mellitus, and obesity) contribute to increased
observed in pregnancy, although no systematic
arrhythmic risk (Figure 1) (4,5,8-10). Obesity is associ-
studies have been powered to accurately determine
ated with developing hypertensive disorders of preg-
these changes. For example, prolonged maximum
nancy, a known risk factor for AF (11,12). Greater
P-wave duration is observed (27). The PR interval
prevalence of cardiovascular disease is also associ-
may shorten, and a leftward shift in the QRS axis
ated with an increased risk of arrhythmias, including
may be seen (28). Prominent Q waves in the inferior
cardiac arrest. A study of 2.2 million pregnancy-
leads and flat and/or inverted T waves in leads III
associated admissions found that cardiac arrest and
and V1-V3 are more frequent in pregnancy. Because
arrhythmias were more common in pregnant women
of modest tachycardia, the QT interval is expected to
with cardiovascular disease than those without car-
be shorter; however, QT and QTc intervals are longer
diovascular disease (0.3% and 7.2% vs 0.004% and
in the second and third trimester of pregnancy
0.3%, respectively) (13). Arrhythmias are the most
compared with nonpregnancy, although they are still
common pregnancy complications in women with
within normal range (29,30). Maximum QTc and the
cardiovascular disease (9.3%) and present earlier in
T-peak to T-end interval, an indicator for dispersion
pregnancy, stressing the need for vigilance in this
of repolarization and sympathetic activation (31),
group (14).
increase by the third trimester. Although these al-
MECHANISMS OF ARRHYTHMIAS IN PREGNANCY terations are observed throughout pregnancy, values
for most women remain within normal physiological
Pregnancy is known to be associated with an ranges (32). However, for patients with an underly-
increased incidence of arrhythmias; more benign ing propensity for repolarization abnormalities,

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122 Tamirisa et al JACC: CLINICAL ELECTROPHYSIOLOGY VOL. 8, NO. 1, 2022

Arrhythmias in Pregnancy JANUARY 2022:120–135

F I G U R E 1 Frequency of Arrhythmias in Pregnancy and Associated Mortality and Complications Between 2000 and 2012

(A) Frequency of any arrhythmia per 100,000 pregnancy-related hospitalizations, stratified by age. (B) Frequency of arrhythmias per 100,000 pregnancy-related
hospitalizations by arrhythmia type. (C) All-cause mortality for the entire study period. (D) Maternal and/or fetal complications by arrhythmia (including preterm labor,
ante- or postpartum hemorrhage, preeclampsia, eclampsia, gestational hypertension, transfusion, postpartum infection, and fluid and electrolyte imbalance). AF ¼ atrial
fibrillation; PSVT ¼ paroxysmal supraventricular tachycardia; PVT ¼ paroxysmal ventricular tachycardia; SVT ¼ supraventricular tachycardia; VT ¼ ventricular tachycardia.
From Vaidya et al (6), with permission.

pregnancy could be a period of vulnerability for
cardiac arrhythmias.
INCIDENCE AND MANAGEMENT OF
SPECIFIC ARRHYTHMIAS
SUPRAVENTRICULAR TACHYCARDIA. Supraventricular
tachycardia (SVT) is 1 of the most common arrhyth-
mias during pregnancy, with a prevalence of 24 per
100,000 admissions. Approximately 20% of patients
with pre-existing SVT have exacerbations during
pregnancy (4). For acute termination, vagal maneu-
vers are the first-line therapy (Central Illustration),
followed by adenosine (33). If adenosine, b-blockers,
or calcium channel blockers are being used for acute
termination of atrioventricular re-entrant tachycardia
in a patient with known pre-excitation, there should
be close monitoring for conversion of atrioventricular
re-entrant tachycardia to pre-excited AF. These
medications can increase conduction over the acces-
sory pathway, which can place the patient at risk of
AF degenerating into ventricular arrhythmias (34).
Flecainide or procainamide can also be used for short-
term termination of SVT in this population. For pa-
tients with recurrent SVT in pregnancy, except for
those with known pre-excitation or history of Wolf-
Parkinson-White syndrome, first-line therapy is b -
blocker therapy, with digoxin and calcium channel
blockers as second-line agents. For long-term sup-
pression of SVT in patients with evidence of pre-
excitation, atrioventricular nodal blockade alone
should be used with caution because of the risk of
development of pre-excited AF and an increased risk
of subsequent conduction over the accessory
pathway (34). Pharmacologic prophylaxis with fle-
cainide can be used for long-term suppression of SVT.

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JACC: CLINICAL ELECTROPHYSIOLOGY VOL. 8, NO. 1, 2022 Tamirisa et al 123
JANUARY 2022:120–135 Arrhythmias in Pregnancy

C ENTR AL I LL U STRA T I O N Arrhythmia Management During Pregnancy for Supraventricular Tachycardia,

Atrial Fibrillation, Ventricular Tachycardia, and Cardiac Arrest

Supraventricular Tachycardia Atrial Fibrillation Ventricular Tachycardia

AVNRT or AVRT • Acute and chronic • Hemodynamically unstable:
Acute: • 1st line: Beta-blockers • Synchronized DC
- Vagal maneuvers ± digoxin cardioversion
- Adenosine* • 2nd line: Ca-channel • Hemodynamically stable
Chronic: blockers • 1st line: lidocaine
• 1st line: Beta-blockers ± • DC cardioversion • 2nd line:
digoxin (in the absence if needed - procainamide
of pre-excitation **) • AADs to prevent - quinidine
• 2nd line: Ca-channel recurrences: • MMVT: Ablation only if
blockers - flecainide refractory with minimal/
• If pre-excitation is - sotalol zero fluoroscopy
present, flecainide + • Ablation, if refractory, • Deferring ablation to
beta-blocker with minimal/zero postpartum is preferred
• Ablation, if refractory, with fluoroscopy • Polymorphic VT: IV Mg
minimal/zero fluoroscopy • Deferring ablation to
• Deferring ablation to postpartum is preferred
postpartum is preferred

Cardiac Arrest Device Management

• Resuscitation/CPR protocol is unchanged • Disable shock therapy on ICDs during
• Manual lateral displacement of uterus labor and delivery, fetal and maternal
• Administration of drugs above the diaphragm to facilitate cardiac monitoring recommended
resuscitation • Devices can be implanted safely with
• Preparation for early cesarean delivery to improve maternal minimal/zero fluoroscopy
and fetal survival • Wearable cardioverter defibrillator
• No medication should be withheld out of concerns for fetal can be used instead of device
teratogenicity implantation
• Drug doses and defibrillation energy protocols remain unchanged

Tamirisa, K.P. et al. J Am Coll Cardiol EP. 2022;8(1):120–135.

Approach to device management is summarized. AAD ¼ anti-arrhythmic drug; AVNRT ¼ atrioventricular nodal reentrant tachycardia; AVRT ¼ atrioventricular tachy-
cardia; Ca ¼ calcium; DC ¼ direct current; ICD¼ implantable cardioverter defibrillator; MMVT ¼ monomorphic ventricular tachycardia.

In cases of hemodynamic instability and concern for
fetal perfusion, urgent electrical cardioversion can be
safely performed (18). Digoxin is contraindicated for
managing atrioventricular re-entrant tachycardia in
the setting of pre-excitation on the resting electro-
cardiogram (34)
Although ablation has been successfully performed
during pregnancy for refractory SVTs using minimal
fluoroscopy (35,36), deferring ablation until the post-
partum period is preferred.
AF AND ATRIAL FLUTTER. AF and atrial flutter are
commonly observed during pregnancy. Most studies
report combined incidences of AF and flutter when
evaluating the presence and treatment of these ar-
rhythmias in pregnancy, which are managed simi-
larly, and little data exists on the prevalence of atrial
flutter alone. In a study of 1,321 pregnant women with
congenital, valvular, and ischemic heart disease
evaluated between 2008 and 2011 in the Registry of
Pregnancy and Cardiac Disease, 1.3% developed AF or
atrial flutter, primarily in the second trimester, with
women with mitral valve disease having a higher
incidence. However, depending on the degree and
type of structural heart disease, the incidences could
be as high as 39.2% (37). The 2020 European AF
guidelines have specific recommendations for

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124 Tamirisa et al
Arrhythmias in Pregnancy
pregnant women, including a class I recommendation
for immediate direct-current cardioversion (DCCV) of
hemodynamically unstable AF and atrial flutter
(18,38). Fetal monitoring is recommended during and
immediately after DCCV (Central Illustration). Beta-
blockers can be used for rate control. Digoxin and
verapamil can be used if needed, but calcium channel
blockers have less supportive data (39). Drug in-
teractions between digoxin and verapamil should be
considered. For rhythm control in the setting of
recurrent or refractory AF, flecainide or sotalol can be
tried.
A new AF or atrial flutter diagnosis should prompt
a transthoracic echocardiogram to evaluate
structural heart disease. In addition, other causes,
such as thyroid disease, electrolyte abnormalities,
pulmonary embolism, and alcohol abuse, should be
considered (38).
If the patient is hemodynamically stable, initial
management involves rate control. However, DCCV is
often desirable for the index episode or inadequate
rate control. DCCV should be performed within 48 h
of AF onset to minimize stroke risk. Transesophageal
echocardiography may be needed if AF onset is un-
clear. Catheter ablation can be performed in re-
fractory symptomatic cases but is generally deferred
until the post-partum period (36,40). The risk of
thromboembolism needs to be considered for preg-
nant patients with AF or atrial flutter; heparin com-
pounds, particularly low-weight-molecular heparin,
are preferred.
Pregnancy is a prothrombotic state, although data
on stroke risk and AF and atrial flutter in pregnancy
are limited. Patients with mitral stenosis should be
fully anticoagulated. CHA 2DS2 -VASC has not been
validated during pregnancy. The 2018 European So-
ciety of Cardiology guidelines recommend the same
criteria for stroke risk stratification as in nonpregnant
patients (41).
VT. Although VT and VF are rare during pregnancy
(with a prevalence of 2 per 100,000 hospital admis-
sions), the risk of recurrent VT in pregnant women
with congenital heart disease is high, at approxi-
mately 27% (42,43).
V T i n s t r u c t u r a l h e a r t d i s e a s e . VT often occurs in
pregnant women with underlying cardiomyopathies,
especially those with nonischemic cardiomyopathies
(44,45). Ischemic cardiomyopathy is uncommon, but
myocardial infarction complicated by ventricular ar-
rhythmias caused by spontaneous coronary artery
dissection and spasm with or without obstructive
disease has been reported (46,47). Patients with
congenital heart disease are at higher risk for VT, with
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JACC: CLINICAL ELECTROPHYSIOLOGY VOL. 8, NO. 1, 2022
JANUARY 2022:120–135
a prevalence of 4.5-15.9 per 1,000 pregnancies (48).
Treatment of VT in patients with structural heart
disease is tailored to the underlying cardiac disease.
Lidocaine and b-blockers can be safely used. Class IC
agents should not be used if VT is caused by coronary
artery disease or myocardial ischemia (49).
VT IN NONSTRUCTURAL HEART DISEASE. VT in the
absence of structural heart disease is typically he-
modynamically stable and associated with a good
prognosis (50). It is often catecholamine sensitive,
and treatment with b -blockers is usually effective
(17). Propranolol or metoprolol should be continued
throughout pregnancy and the post-partum period
for
(51,52). Sotalol, flecainide, or quinidine may be
considered in symptomatic patients with VT that re-
curs despite b-blocker therapy. Verapamil can be
used for acute termination and prevention of fascic-
ular VT (53).
A c u t e t r e a t m e n t o f V T i n p r e g n a n c y . In the
setting of hemodynamic instability, DCCV should be
performed emergently because of the high risk of
fetal compromise. DCCV at 50-100 J (and if needed,
higher energies at 100-360 J) can be used (54). If the
patient is hemodynamically stable, lidocaine should
be tried first (54). Procainamide or quinidine may be
used if lidocaine is ineffective (Central Illustration).
Amiodarone can be used in life-threatening situations
when other therapies have failed (55). Magnesium
(1-2 g intravenously) can be safely used for torsade de
pointes or polymorphic VT (54). Although case re-
ports of successful ablation have been reported (56),
VT ablation is considered an option of last resort (57).
CARDIAC ARREST IN PREGNANCY
Maternal cardiac arrest is a complex phenomenon
that appears to be rising in frequency, occurring in
approximately 1 per 12,000 hospitalizations (58).
Hemorrhage and anesthetic complications are the
most prevalent causes of cardiac arrest that require
cardiopulmonary resuscitation (CPR), but cardiovas-
cular causes should also be considered (59). Heart fail-
ure, acute myocardial infarction, sudden cardiac arrest
(SCA) death, aortic dissection, and pulmonary edema
are the most common cardiopulmonary causes of SCA
(7). Arrhythmias contribute to a substantial proportion
of events (7,60). Because of the underlying causes of
arrest in pregnancy tend to be reversible (because of
sepsis or hemorrhage), and because of increased
monitoring during pregnancy, better outcomes after
SCA for pregnant women than nonpregnant women
have been observed (61). The hormonal changes during
pregnancy may also improve myocardial and cerebral
JACC: CLINICAL ELECTROPHYSIOLOGY VOL. 8, NO. 1, 2022
JANUARY 2022:120–135
blood flow during CPR (61). Notably, African American
women have the highest mortality compared with
other racial/ethnic groups (61).
Cardiac arrest and especially postarrest care of the
mother and the fetus benefit from a multidisciplinary
team of maternal and fetal experts, including anes-
thesiologists, cardiologists, obstetricians, and neo-
natologists. During cardiopulmonary resuscitation
and to avoid aorto-caval compression at 20 weeks of
gestation and beyond, manual lateral displacement of
the uterus should be considered. Chest compressions
are performed in the standard position on the ster-
num. Preparation should be made for early peri-
mortem and/or emergency cesarean delivery. No
medication should be withheld out of concerns for
fetal teratogenicity. Drug doses and defibrillation
protocols remain unchanged. Fetal monitoring may
be interrupted during emergent management.
INHERITED ARRHYTHMIA SYNDROMES
Pregnancy in women with inherited arrhythmia syn-
dromes is generally safe. Disease-specific assessment
includes risk stratification, evaluation of potential
peripartum triggers, and pharmacologic manage-
ment. Prepregnancy genetic counseling, optimization
of drugs, electrocardiography and exercise testing,
echocardiography, and implantable cardioverter-
defibrillator (ICD) optimization and/or monitoring
from the prepartum to the postpartum period are
important. Labor and delivery planning, review of
drugs postpartum, and cardiology assessment for the
newborn should occur as part of a multidisciplinary
approach (62).
Long QT syndrome is the most common inherited
arrhythmia syndrome. Established risk factors for
arrhythmias include a history of previous arrhyth-
mias and QTc >470 ms. The risk of arrhythmic
events in women with long QT syndrome is not
significantly elevated during pregnancy compared
with a control period before pregnancy (63,64).
However, the arrhythmic risk is markedly elevated
in the 9-month postpartum period (63,64), particu-
larly among women with long QT syndrome type 2
(63-65). Adrenergic triggers are most relevant for
long QT syndrome type 1, posing an increased risk
around the time of labor and delivery (66). Auditory
stimuli and loud noises are important triggers of
arrhythmias for long QT syndrome type 2 and should
be avoided. Lactation is generally considered safe
and does not need to be avoided in patients with
long QT syndrome. Beta-blockers are highly effective
at preventing arrhythmic events and should be
continued in all pregnant patients with this
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Tamirisa et al 125
Arrhythmias in Pregnancy
syndrome, especially through the high-risk post-
partum period (64,65). The nonselective b -blocker
propranolol is preferred, because of the greater
experience with the safety of this drug. If VT is
already effectively controlled on nadolol, the drug
can be continued throughout pregnancy. There is a
potentially greater risk for fetal adverse events with
atenolol; therefore, atenolol should be avoided. In
cases refractory to b -blocker therapy, particularly for
long QT syndrome types 2 and 3, the addition of
mexiletine can be considered. Fetal echocardiogra-
phy should be considered. Particular attention
should be paid to anti-emetic use in pregnant
women with long QT syndrome because most anti-
emetics prolong the QT interval (66). Close atten-
tion should be paid to avoiding other QT-prolonging
medications, including anti-emetics (eg, ondanse-
tron) and agents that may typically be used for
anesthesia (ie, sevoflurane). A comprehensive list
can be found at https://www.crediblemeds.org. Of
note, oxytocin can prolong QT. Therefore, close co-
ordination among obstetrics, obstetric anesthesia,
and pharmacy services is crucial to achieving good
outcomes.
Less common inherited arrhythmia syndromes
during pregnancy include catecholaminergic poly-
morphic VT, Brugada syndrome, and arrhythmogenic
right ventricular cardiomyopathy. Arrhythmic events
in catecholaminergic polymorphic VT are triggered by
physical exertion or emotional stress, both of which
may be relevant during labor and delivery. However,
the risk of arrhythmic events in pregnant women with
this disorder does not appear to be elevated
compared with prepregnancy (67). Nonselective b-
blockers play a key role in managing ventricular ar-
rhythmias in catecholaminergic polymorphic VT. It is
important that they are continued throughout preg-
nancy and in the postpartum period. Flecainide may
be used if events occur despite b-blocker therapy (66).
Brugada syndrome is much more common in men,
and data on managing this syndrome in pregnancy
are limited. Arrhythmic events in Brugada syndrome
typically occur during periods of high vagal tone, and
treatment with quinidine can effectively reduce
arrhythmic events in pregnancy (68). Pregnancy in
women with arrhythmogenic right ventricular car-
diomyopathy is generally well-tolerated. Beta-
blockers should be continued during pregnancy,
particularly in patients with a history of ventricular
arrhythmias. Although arrhythmogenic right ventric-
ular cardiomyopathy typically shows a predilection
for the right ventricle, pregnancy is contraindicated
in rare cases of biventricular involvement and left
ventricular ejection fractions of <30% (66).
126 Tamirisa et al
Arrhythmias in Pregnancy
T A B L E 1 Previous Food and Drug Administration Pregnancy
Categories for Drugs
A No fetal risk in controlled studies
B No risk to human fetus despite possible animal risk or no risks
in animal studies but human studies lacking
C Human risk cannot be ruled out. Animal studies may or may not
show risk
D Evidence of risk to human fetus
X Contraindicated in pregnancy
GENERAL MANAGEMENT OF ARRHYTHMIAS
IN PREGNANCY
ANTIARRHYTHMIC DRUGS AND RATE-CONTROLLING
MEDICATIONS. The primary concern regarding drugs
during pregnancy is the potential for fetal adverse
effects and teratogenicity, which are greatest during
organogenesis (5-10 weeks after conception). The U.S.
Food and Drug Administration rating for drugs in
pregnancy (A to X) (Table 1) is no longer being used
and has been replaced by a narrative risk. Random-
ized clinical trials evaluating the effects of antiar-
rhythmic drugs (AADs) in pregnancy are lacking;
therefore, careful assessment of efficacy and safety
should be performed before initiation, and the lowest
effective dose used.
B e t a - b l o c k e r T h e r a p y . Significant experience with
b-blocker therapy for treatment of maternal hyper-
tension, channelopathies, and cardiomyopathies ex-
ists during pregnancy. These medications cross the
placenta, and long-term treatment is associated with
a small risk of fetal growth retardation (69). Large
registries of pregnant patients exposed to b-blockers
reported no increased risk of congenital malforma-
tions after adjusting for maternal comorbidities
(70,71). In a propensity-matched analysis, b-blocker
use versus placebo was associated with a 4.3% risk
versus 1.2% risk of neonatal hypoglycemia and a 1.6%
risk versus 0.5% risk of neonatal bradycardia (72).
Propranolol and metoprolol are preferred (Figure 2)
(73-76). Nadolol and pindolol have also been safely
used in pregnancy. Atenolol, which has decreased
protein binding, has shown a greater risk of fetal
adverse effects (Table 2) (77-82). Atenolol may be
excreted at higher levels in breast milk and is not
recommended during lactation (Figure 2).
C a l c i u m c h a n n e l b l o c k e r s . Verapamil has been
used without significant risk of teratogenicity,
although maternal hypotension and fetal bradycardia
have been reported (54). Use of diltiazem is more
controversial because of the fetal adverse effects
noted in animal models (83,84). In observational
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JACC: CLINICAL ELECTROPHYSIOLOGY VOL. 8, NO. 1, 2022
JANUARY 2022:120–135
studies, there was a trend toward decreased neonatal
birth weight and increased rates of preterm delivery
with calcium channel blockers versus matched con-
trol subjects (23.8% vs 6.5%) (85,86). Verapamil
and diltiazem are compatible with lactation (Figure 2).
For the short term, calcium channel blockers should
be avoided if adenosine can be used. If necessary,
verapamil, up to 10 mg intravenously, has not
been associated with significant fetal hemodynamic
effects (87).
C l a s s I A A A D s . Quinidine and procainamide cross
the placenta and do not have teratogenic effects but
can cause torsade de pointes. Adverse events such as
thrombocytopenia with quinidine and drug-induced
lupus with procainamide should be considered.
Quinidine has a long track record of safety with only
rare reported fetal adverse effects (Table 2) (41,88).
Electrophysiologists with experience using this
medication should follow patients treated with
quinidine. Quinidine levels should be monitored, and
potential drug-drug interactions, especially with
digoxin, need to be considered. Quinidine should be
avoided during lactation, because of the accumula-
tion of the drug in the immature neonatal liver. Pro-
cainamide has been used without reported
teratogenic effects for the treatment of VT in preg-
nancy, although data are limited (89,90).
C l a s s I B A A D s . Lidocaine has a well-established
safety profile in pregnancy. Levels should be moni-
tored to avoid toxicity. Lidocaine crosses the
placenta, but at therapeutic doses, no effects on
uteroplacental circulation, amniotic fluid pressure, or
fetal heart rate in animal models have been observed
(91,92). Data from the Collaborative Perinatal Project
suggested that exposure to lidocaine early in preg-
nancy was not associated with an increased risk of
birth defects or adverse events, with an overall
normal perinatal course (90). Like lidocaine, mex-
iletine does cross the placenta and is found in
breastmilk. Although there have been case reports of
mexiletine use in pregnancy, additional data are
needed (Table 2) (93,94). Lower Apgar scores have
been reported with mexiletine, and in animal models,
increased risk of fetal resorption at 4 maximum
recommended human doses has been observed.
Levels should be monitored.
C l a s s I C A A D s . Flecainide has been safely used to
treat maternal and fetal arrhythmias (41), although
rarely, neonatal toxicity can occur (95). Initiation of
flecainide (300 mg/day) is generally safe and can
improve fetal mortality in the setting of fetal SVT
(96). Animal data in rodents at 50-80 mg/kg/day have
confirmed no teratogenic effects (Table 2) (41).
JACC: CLINICAL ELECTROPHYSIOLOGY VOL. 8, NO. 1, 2022 Tamirisa et al 127
JANUARY 2022:120–135 Arrhythmias in Pregnancy

F I G U R E 2 Safety Profiles of Commonly Used Medications for the Treatment of Arrhythmias in Pregnancy

Background colors refer to safety profiles of medications based on data and experience in pregnancy. Medications that can be safely used in
lactation are also indicated separately by an icon. Figure 2 was created with assistance from Biorender.com.

There are minimal data on propafenone use in
pregnancy. No neonatal adverse outcomes were re-
ported in single case reports for Wolf-Parkinson-
White syndrome, SVT, and premature ventricular
contractions (97-99). Propafenone and its metabolite
cross the placenta. Metabolite concentration may be
higher in the cord than in the plasma. Propafenone is
also found in breast milk (98). Propafenone is not
teratogenic, but in animal models, fetal adverse
events were noted at 3-6 maximum recommended
human doses (Table 2) (41).
C l a s s I I I A A D s . Among class III agents, sotalol is
considered safe during pregnancy and lactation,
with only a small risk of fetal bradycardia and hy-
poglycemia. No teratogenic effects were observed in
animal models (41). Bioavailability and clearance of
oral sotalol during pregnancy is not significantly
altered during pregnancy, although it is more rapidly
cleared after intravenous administration during
pregnancy compared with the postpartum period
(6.6 h vs 9.3 h) (100). Dronedarone should not be
used in pregnancy or lactation because it causes
significant adverse events. Amiodarone should also
be avoided, unless no other option is available, and
then used for as short of a duration as possible
(Table 2, Figure 2). In a study of 26 fetal incessant

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128 Tamirisa et al JACC: CLINICAL ELECTROPHYSIOLOGY VOL. 8, NO. 1, 2022

Arrhythmias in Pregnancy JANUARY 2022:120–135

T A B L E 2 Arrhythmia Medications and Adverse Events in Pregnancy

Drug VW Class Previous Category Fetal Adverse Effects

Quinidine IA C Long track record of safety. No teratogenicity observed. Rarely, mild uterine contractions,
premature labor, neonatal thrombocytopenia, and cranial nerve VIII damage has been
reported.
Procainamide IA C Minimal human and animal data.
Lidocaine IB B Long track record of safety in humans and animal models.
Mexiletine IB C Minimal data. Concern for lower Apgar scores. Increased fetal resorption at 4 maximum
RHD in rats and rabbits.
Flecainide IC C Long track record of safety for fetal arrhythmias. At very high doses, delayed sternal and
vertebral ossification observed in rats.
Propafenone IC C Minimal human data. Reduction in neonatal survival, weight gain, and development
abnormalities observed at 3-6 maximum RHD.
Propranolol II C No significant adverse effects. Small risk of FGR, neonatal bradycardia, and hypoglycemia.
Metoprolol II C No significant adverse effects. Small risk of FGR, neonatal bradycardia, and hypoglycemia.
Pindolol II B No significant adverse effects.
Nadolol II C Small risk of apnea, FGR, and hypoglycemia
Atenolol II D Greater risk of FGR and fetal bradycardia compared with other b-blockers, other b -blockers
are preferred over atenolol.
Carvedilol II C No adequate data on adverse effects, not used in pregnancy.
Sotalol III C No teratogenic potential. Small risk of fetal bradycardia and hypoglycemia. In rats and
rabbits, at 9 and 7 maximum RHD, teratogenic effects were not observed.
Amiodarone III D Significant adverse effects, including fetal hypothyroidism, growth retardation, and
prematurity. Used in pregnancy only if other options are not available.
Dronaderone III X Significant fetal adverse events including vascular and limb abnormalities and cleft palate.
Avoid in pregnancy.
Dofetilide III C Human data lacking. In pregnant rats, caused fetal resorption and skeletal abnormalities if
administered during organogenesis. In rats, dofetilide caused significant bradycardia at
gestational days 11 and 13, even at the lower doses of 2.5 mg/kg.
Ibutilide III C Minimal human data. No adverse events reported in case reports. Increased IKr inhibition and
risk of TdP. In rats, skeletal and cardiac abnormalities noted with daily exposure at
4 RHD.
Verapamil IV C Trend toward decreased FGR, maternal hypotension, and fetal bradycardia have been
reported. Maternal hemodynamic instability if infused rapidly. No teratogenicity is
observed at 1.5 RHD in rabbits and 6 maximum RHD in rats.
Diltiazem IV C Increased risk of FGR. Skeletal, cardiac, tongue, and retinal abnormalities in animal models. At
4-6 RHD, embryo and fetal lethality in mice, rats, and rabbits.
Adenosine NA C No significant adverse events. Consider fetal monitoring, possible small risk of transient fetal
bradycardia.
Digoxin NA C No significant adverse effects. Monitor maternal levels for toxicity.
Ivabradine NA NA Exposure at near therapeutic doses shows high incidence of fetal cardiac defects in rats and
ectrodactyly in rabbits. FGR, neonatal bradycardia, and hypotension can occur. Avoid in
pregnancy.
Atropine NA C No adequate data

FGR ¼ fetal growth retardation; RHD ¼ recommended human doses; TdP ¼ torsade de pointes

tachycardias or hydrops fetalis (gestational age 23-
31 weeks) for whom digoxin and other AADs were
not effective, use of amiodarone (duration of use 1-
15 weeks) converted most of the fetal tachycardias,
without significant permanent fetal adverse effects
(101). Data on dofetilide in pregnancy are lacking.
Because of the rapid delayed rectifier potassium
channel inhibition, it is not recommended. Brady-
cardia and skeletal abnormalities
observed in animal models (Table 2) (102,103). Data
on ibutilide are restricted to a few case reports for
atrial flutter/AF cardioversion. No adverse fetal ef-
fects were reported. In these case reports, mothers
received pretreatment with magnesium (104,105).
Rat studies have shown teratogenic effects at
4 recommended human doses RHD with ibutilide
(Table 2) (106).
Other arrhythmia m e d i c a t i o n s . Because of its
short half-life, adenosine is safe and the preferred
medication to terminate maternal SVT in pregnancy
(Figure 2). One case report found a detectable short-
lived effect on fetal cardiac rhythm, whereas several
others, including a case series of 33 pregnant patients
have been with 38 SVT episodes, did not note any fetal effects
(33,107-109). Starting dose should be 6-12 mg.
Although pregnancy reduces adenosine deaminase,
the increased intravascular volume may counter
these effects.
Digoxin has a long history of safety in pregnancy
(110,111). Digoxin concentrations are similar in the

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JACC: CLINICAL ELECTROPHYSIOLOGY VOL. 8, NO. 1, 2022
JANUARY 2022:120–135
mother and newborn (112). Both blood levels and
clinical signs of digoxin toxicity should be assessed
because the measurement of levels in pregnancy can
be compromised by the circulation of digoxin-like
fragments that may falsely increase levels (113).
Although digoxin is excreted in breast milk, the dose
ingested by infants is small and of little significance
(110,114).
Atropine has been used for emergent resuscitation
in pregnancy, but little data exist regarding its safety
profile. Finally, ivabradine is contraindicated in
pregnancy and lactation, because of teratogenicity in
animal models and the risk of fetal growth retardation
and neonatal hemodynamic compromise.
ELECTRICAL CARDIOVERSION
Acute DCCV in pregnancy is warranted in cases of
hemodynamic instability or when rate control is un-
successful (115). Secondary causes like congenital
heart disease, valvular disease, alcohol abuse, medi-
cations (eg, terbutaline), electrolyte imbalance, and
hyperthyroidism should be ruled out. Cardioversion
does not compromise blood flow to the fetus but can
cause uterine contractions (116). The risk of inducing
fetal arrhythmias is small, and there is a theoretical
risk of preterm labor with electrical intervention (54).
Fetuses of mammals have high defibrillation thresh-
olds, and the overall current that reaches the uterus is
small. However, amniotic fluid is a good conductor
(117), so fetal monitoring is suggested (118). Energies
ranging from 50-400 J have been used without fetal
adverse effects and has shown success rates of >90%
(24,119). Defibrillation pads should be placed away
from the gravid uterus. It is prudent to care for these
patients in centers with the capacity to undertake
emergency C-sections if needed (54).
ANTICOAGULATION
Anticoagulation for arrhythmias in pregnancy, such
as AF, is not well-studied, and no formal recommen-
dations exist. Most data, therefore, have been inter-
polated from pregnant patients with mechanical
heart valves. Low-dose aspirin is considered safe
throughout pregnancy (120,121). Warfarin crosses the
placenta and can be used at doses of <5 mg/day
during the first trimester and >5 mg/day during the
second trimester (class IIa recommendation in the
European Society of Cardiology 2018 guidelines) (41).
Higher doses of warfarin are associated with a 15%-
56% risk of miscarriage and a 30% risk of congenital
anomalies (122). Warfarin is switched to unfractio-
nated heparin or low-molecular-weight heparin at the
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Tamirisa et al 129
Arrhythmias in Pregnancy
36th week of gestation, and this transition requires
hospitalization and inpatient management (41). Low-
molecular-weight heparin and unfractionated
heparin do not cross the placenta (123,124). Frequent
laboratory testing is recommended with dose adjust-
ment as needed. Low-molecular-weight heparin has a
better safety profile, with fewer side effects (eg,
thrombocytopenia, bleeding, and osteoporosis) (125).
In pregnancy, a higher anticoagulant dose with more
frequent administration of unfractionated or low-
molecular-weight heparin is required to maintain
therapeutic levels because of the increased plasma
volume, glomerular filtration rate, and placenta
degradation heparinase. For full-dose anti-
coagulation, low-molecular-weight heparin should be
given subcutaneously (100 U/kg twice daily) and the
dose adjusted to maintain the anti-Xa level between
0.5 and 1.0 U/mL, 4-6 h after injection. Unfractio-
nated heparin is adjusted to target the mid-interval
activated partial thromboplastin time in the thera-
peutic range (1.5-2.5 times mean reference range).
Unfractionated or low-molecular-weight-heparin
should be discontinued 12 h before planned induc-
tion of labor. To minimize bleeding, resumption of
anticoagulation should be postponed until 12 h after
vaginal delivery, 2-12 h after epidural removal, or 24 h
after cesarean delivery (125). Heparin or low-
molecular-weight heparin should be overlapped
with warfarin for 4-5 days (123,124,126).
There are minimal data on the use of direct-acting
oral anticoagulants in pregnancy, which are known to
cross the placenta. In an analysis of the World Health
Organization’s VigiBase database, which consists of
16 million individual case reports of suspected drug
reactions across 131 countries, and after confounding
factors and alternative causes were excluded, no
statistically significant association for the use of
rivaroxaban with spontaneous abortion was found.
However, apixaban use was associated with an
increased probability of spontaneous abortion
compared with warfarin (127). Fetal concentrations of
apixaban may range from 35% to 90% of maternal
concentration levels, with the potential for direct
fetal toxicity (127).
CATHETER ABLATION
Catheter ablation using electroanatomic mapping
systems and intracardiac ultrasound to reduce fluo-
roscopic exposure (“zero-fluoroscopy”) has been
safely performed during pregnancy in experienced
centers for drug-refractory and poorly tolerated ar-
rhythmias (36,128,129). Deferring ablation to post-
partum preferred. In a meta-analysis of 27 cases,
130 Tamirisa et al
Arrhythmias in Pregnancy
successful ablation was reported in all cases, despite
reduced left ventricular function in 9 of 27 patients. A
case of microcephaly and a case of maternal pre-
eclampsia and placental abruption that led to early
cesarean delivery at 27 weeks, 5 weeks after ablation,
were reported (129). For an ablation procedure, the
patient should be placed in the left lateral tilt position
to prevent aortocaval compression, especially after
the second trimester of pregnancy. Continuous fetal
monitoring is important, particularly if cesarean de-
livery is an option, depending on the fetal gestational
stage (>24 weeks). Most fetal effects caused by radi-
ation occur before 17 weeks of gestation at fetal doses
of ionizing radiation >200 mGy (130). Exposure
of <50 mGy has not been associated with fetal ab-
normalities (131). Radiation exposure between 8 and
45 weeks of 60 to 310 mGy may result in mental
retardation (132). Lifetime risk of malignancy is low,
although casecontrol studies have suggested that
antenatal exposure as little as 10 mGy may increase
the risk of childhood cancer (133). In general, the fetal
radiation dose is estimated to be <1 mGy based on
analysis of ablation data in healthy women who have
undergone SVT ablation. At this dose, the estimated
average excess fatal cancer risk is 14.5 per 10 million
unborn children who received radiation during the
first postconception weeks and 30 and 55.6 per 10
million fetuses that received radiation in the second
and third trimesters, respectively (134).
IMPLANTABLE DEVICE MANAGEMENT
IN PREGNANCY
The presence of previously implanted pacemakers and
ICDs in pregnant women do not increase maternal or
fetal risk (135,136). For women who develop in-
dications for device implantation during pregnancy,
devices can be implanted safely with minimal fluo-
roscopy and under echocardiographic guidance and
electroanatomic mapping (137,138). Routine device
monitoring, comanagement with cardiologists/cardiac
electrophysiologists, and follow-up should
continued throughout the peripartum period.
PACEMAKERS. Bradyarrhythmias during pregnancy
are predominantly observed in women with congen-
ital heart disease. The true incidence of sinus node
dysfunction in pregnancy is unknown, and pregnancy
is not predisposed to high-grade atrioventricular
block. QRS prolongation in pregnancy may be due to
ventricular dilatation, clinical implications of which
are unclear.
Indications for pacemaker implantation, including
for symptomatic bradycardia, remain unchanged.
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JACC: CLINICAL ELECTROPHYSIOLOGY VOL. 8, NO. 1, 2022
JANUARY 2022:120–135
Because of the demand for increased heart rate, rate
response can be programmed to treat chronotropic
incompetence or sinus node dysfunction as the
pregnancy progresses. Most patients with pace-
makers have an uneventful pregnancy from the
pacemaker perspective. A study of only 11 pregnant
patients with pacemakers reported maternal compli-
cations in 3 patients (136). However, none of these
complications had a plausible direct connection to the
device itself. Vaginal delivery is not a contraindica-
tion with a maternal pacemaker, and pacemakers do
not interfere with fetal monitoring. Reprogramming
the pacemaker to an asynchronous mode during
caesarian delivery and using bipolar cautery in
pacemaker-dependent patients is important to avoid
pacing inhibition caused by noise interference (139).
Skin irritation at the pacemaker site because of breast
hypertrophy has been reported (140).
ICDs. Incidence and overview of VT and cardiac ar-
rest management have been discussed previously; it
may be advisable, although not required, to disable
shock therapy on ICDs during labor and delivery,
assuming adequate maternal cardiac monitoring is in
place. This recommendation may be particularly
relevant for pregnant women with subcutaneous de-
fibrillators, which are susceptible to oversensing and
may result in inappropriate shocks from oversensed
uterine contractions or myopotentials during labor
and delivery (66).
For patients with clear indications for defibrillators
during pregnancy, subcutaneous defibrillators can
also be implanted without fluoroscopy. However,
experience with implantation in pregnant women and
the impact of pregnancy on device sensing is limited.
Wearable cardioverter-defibrillators have emerged as
an alternative for patients with transient arrhythmic
risk or as a bridge to ICD implantation. However, data
on the efficacy of wearable cardioverter-defibrillators
at terminating VT during pregnancy are lacking.
TREATMENT OF FETAL ARRHYTHMIAS
be IN PREGNANCY
Fetal arrhythmias include premature atrial con-
tractions, premature ventricular contractions,
tachyarrhythmias, and bradyarrhythmias. Electro-
cardiography, cardiotocography, echocardiography,
and magnetocardiography can be used for moni-
toring (141).
ECTOPIC BEATS. Most premature atrial and ventric-
ular contractions are benign and require no inter-
vention. However, close follow-up with weekly
Doppler assessment is recommended because
JACC: CLINICAL ELECTROPHYSIOLOGY VOL. 8, NO. 1, 2022 Tamirisa et al 131
JANUARY 2022:120–135 Arrhythmias in Pregnancy

sustained arrhythmias can be seen in 1%-3% of fetal prematurity and postnatal pacing must be considered.
cases (141). Evaluation by a fetal cardiologist to rule Postnatal surgery and pacemaker implantation are
out structural heart disease is recommended. In a helpful for cases associated with congenital heart
retrospective series, the occurrence of second-degree disease (153).
atrioventricular block was associated with long QT Congenital complete heart block (incidence of 1
syndrome or maternal anti-Rho or anti-La antibodies in 15,000 live births) may be associated with
(142). maternal autoantibodies against SSA (Ro) or SSB
(La) proteins (neonatal lupus syndrome) or second-
TACHYARRHYTHMIAS. Persistent tachyarrhythmias,
ary to cardiac malformations (eg, congenital atrio-
defined as fetal heart rates >180 beats/min, are rare
ventricular canal defects) (154). Heart block
and occur in <0.1% of all pregnancies (143). Fetal si-
resulting from neonatal lupus syndrome is usually
nus tachycardia is seen with maternal fever, maternal
identified between 18 and 28 week of gestational
thyrotoxicosis, infection, stimulants, anemia, and
age and is associated with high fetal mortality (155).
fetal distress (143). Treatment involves treating the
Maternal administration of immunosuppressive
underlying cause. Atrial flutter and SVTs account for
medications (dexamethasone or betamethasone) has
26.2% and 73.2% of fetal tachyarrhythmias, respec-
shown modest benefit. In a study of 21 patients
tively (144). Management involves close monitoring,
treated with dexamethasone, the 1-year fetal sur-
transplacental drug therapy, and delivery of the fetus
vival rate was 90% versus 46% without glucocorti-
(145). Treatment of SVT is based on the persistence of
coid therapy (156). Episodes of transient bradycardia
the rhythm, gestational age, presence of structural
are benign and typically resolve with fetal activity.
heart disease, and fetal well-being. Intermittent fetal
Ambulatory surveillance programs and wearable
tachycardia is well tolerated and can be monitored
fetal heart rate monitors may afford early identifi-
with weekly and/or biweekly ultrasounds without
cation of evolving fetal heart block, allowing for
any therapy, in the absence of hydrops or congenital
emergent treatment. There is also preliminary data
heart disease. Sustained tachyarrhythmias are asso-
that suggests a role in preventing congenital com-
ciated with a high incidence (35%-40%) of fetal
plete heart block with hydroxychloroquine,
hydrops (144). In case of persistent rhythms, digoxin
although additional data are needed (157). To date,
is the first line of therapy. Flecainide and sotalol are
implementing fully implantable fetal micro-
second-line agents. Transplacental treatment with
pacemakers via a minimally invasive approach for
digoxin, sotalol, and flecainide is effective in 89.8%
congenital complete heart block in utero to treat
of fetal cases with persistent SVT, with the resolution
fetal hydrops remains challenging (158).
of fetal hydrops in 75% of cases. In a small study,
maternal adverse events, including nausea/vomiting,
CONCLUSIONS
headaches, atrioventricular Wenckebach, and PR in-
terval prolongation were observed with serious
Maternal mortality has risen over the past 2 decades
adverse events in 1 mother and 4 fetuses, which
in the United States. Although the exact association
resulting in 2 fetal deaths caused by heart failure
of arrhythmias with maternal mortality is unclear, an
(146). Other medications, such as propranolol and
increasing incidence of arrhythmias over the same
procainamide, can also be used; amiodarone is a drug
period, associated with a growing incidence of pre-
of last resort (96,101,147-150).
existing cardiovascular and congenital heart disease,
VT is infrequent and seen in the setting of under-
advanced age, and comorbidities, has been observed,
lying structural and/or conduction abnormalities,
making an in-depth understanding of arrhythmia
such as complete heart block, fetal myocarditis, or
management in pregnancy critical. Specific AADs and
genetic conditions such as long QT syndrome. Trans-
cardiac medications can be used to treat or prevent
placental therapy with lidocaine and magnesium,
arrhythmias in pregnancy, and catheter ablation may
mexiletine, and b-blockers have been reported (151).
be used safely, with minimal fluoroscopy, when
BRADYARRHYTHMIAS. Persistent fetal bradycardia is medical therapy has failed. However, much of the
rare, defined as a fetal heart rate of <100 beats/min, data regarding management strategies for arrhythmia
and is associated with fetal distress, hypoxia, acidosis, treatment in pregnancy is derived from observational
congenital long QT syndrome, and sinus node studies and case series, delineating a clear need for
dysfunction. Administration of b -sympathomimetics, larger studies and randomized clinical trials. Preg-
such as oral terbutaline, has been reported, but it is nant women with significant arrhythmias require a
unclear if this treatment improves fetal survival (152). multidisciplinary approach, including at the time of
Preterm delivery is an option for hydrops, but labor and delivery. In addition, prenatal counseling

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132 Tamirisa et al JACC: CLINICAL ELECTROPHYSIOLOGY VOL. 8, NO. 1, 2022

Arrhythmias in Pregnancy JANUARY 2022:120–135

regarding the high risk of arrhythmia recurrence
during pregnancy, consideration of ablation before
pregnancy, and close monitoring in high-risk patients
can be essential for successful maternal and fetal
outcomes.
a consultant for Atricure, Biosense Webster, and Medtronic. Dr
Volgman has been a MSD/Bayer Virtual Global Advisory Board
Member; has been a member Bristol Myers Squibb Foundation of the
Diverse Clinical Investigator Career Development Program; has been a
member of the National Advisory Committee; and holds stock in
Apple. Dr Vaseghi holds stock in Secures Inc.

FUNDING SUPPORT AND AUTHOR DISCLOSURES ADDRESS FOR CORRESPONDENCE: Dr Marmar

Dr Vaseghi was supported by NIH R01 HL148190. Dr Mason has been a
consultant for Medtronic and Boston Scientific. Dr Russo has received
research funding from or has been a member of steering committees
for Boston Scientific, Kestra, Medilynx, and Medtronic; and has been
Vaseghi, UCLA Cardiac Arrhythmia Center, University
of California, 100 Medical Plaza, Suite 660, Los
Angeles, California 90095, USA. E-mail: mvaseghi@
mednet.ucla.edu.

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KEY WORDS arrhythmias, fetal,
peripartum, pregnancy